Transferred T cells preferentially adhere in the BALT of CD26-deficient recipient lungs during asthma.

The multifunctional glycoprotein CD26/dipeptidyl peptidase 4 (DP4) has a DP activity, plays a role during T-cell activation, and interacts with several proteins, including extracellular matrix (ECM)-proteins. The latter have been studied mainly in the context of experimental metastasis. The potential role of CD26 for T-cell adhesion could be of major interest. Here, a coisogenic transfer of CFSE-labelled T cells was performed after isolation from CD26-expressing or CD26-deficient F344 rat donors and subsequent cross-transfer to recipients of the other substrain. Their recovery in the lungs was quantified using flow cytometry, a histochemical activity assay, as well as immunohistochemistry and morphometry. Under naive conditions there were neither differences in the numbers of recovered T cells nor in their preferential anatomical sites of adhesion. The induction of an asthma-like inflammation, however, led to a site-preferential adhesion of T cells in the bronchus-associated lymphatic tissue (BALT). In this compartment of the lungs, surprisingly, significantly more T cells were found in CD26-deficient recipient lungs, regardless of the origin of the transferred T cells. These findings demonstrate a negative regulatory role of the BALT-specific expression of CD26 in T-cell adhesion during an asthma-like inflammation. Considering the pattern of cellular re-distribution it is not very likely that CD26 expressed on T cells and/or endothelial cells represents a significant factor in T-cell adhesion in vivo. Instead, the present findings suggest that the lack of the CD26 peptidase function in BALT might cause an overflow of a T-cell chemoattractant, which yet remains to be identified.